# Targeting Glucose Metabolism with HJC0152 for Treating Metastatic Breast Cancer

> **NIH NIH R01** · LSU HEALTH SCIENCES CENTER · 2020 · $1

## Abstract

The majority of breast cancer (BC)-associated deaths are a direct result of invasive progression and
metastasis developed in other organs such as the brain, bones, lungs, or other organs. An estimated 50 -80% of
invasive BC patients will develop metastasis, resulting in a sharp decrease of 5 -year survival rate from 99% in
patients with localized BCs to 27% in patients with distant metastasis. The only available targeted therapies for
metastatic BCs (MBCs) are Selective Estrogen Receptor (ER) Modulators (SERMs) and Aromatase Inhibitors
(AIs), which are only effective in about half of ER-positive BC patients. There are currently no other available
targeted therapies for nonresponsive/resistant ER-positive BCs and all ER-negative BCs. These facts manifest the
urgent need for identifying non–ER-based molecular targets and developing targeted therapies to block the
progression of various subtypes of BCs to metastatic diseases. BC cells have abnormal glycolysis and the
proliferating BC cells rely on dysregulated glycolysis, therefore sensitive to inhibition of glycolysis. Triple-
negative BC (TNBC), the most aggressive and highly metastatic subtype of BC, was found to have increased
glucose uptake, thus supporting the notion that disturbance in glucose metabolism is linked to TNBC
carcinogenesis. Therefore, development of agents targeting aberrant glucose metabolism may offer alternative
and potentially more effective approach for treating metastatic BC (MBC). To address this pressing need, we
recently developed HJC0152 as a putative glucose metabolism modulator for treating MBCs and as molecular
tool to elucidate the metastasis determinants and associated mechanisms that drive BC metastatic progression. In
preliminary studies, HJC0152 was found to suppress cancer progression, inhibit cancer cell motility, block lung
metastasis development, and inhibit tumor local invasion. Our central hypothesis is that HJC0152 targets key
metabolism enzyme(s) to modulate glucose metabolism and suppress BC cell motility and BC metastatic
progression. Three specific aims are proposed. In Aim 1, we will assess HJC0152’s efficacy in regressing the
growth of MBCs, blocking lung metastasis development from MBCs, and prolonging the lifespan of MBC -
bearing animals in vivo. In Aim 2, we will assess HJC0152-targeted metastasis determinant proteins and optimize
HJC0152 to enhance the overall drug development profiles. In preliminary studies, we have identified high -
confidence targets including ARG that may directly interact with HJC0152. In Aim 3, we will define and validate
key metastasis determinant proteins mediating the anti-metastatic effect of HJC0152. The ultimate goal is to
develop an innovative, non–ER-based therapy to inhibit existing metastasis and reduce/block new metastasis to
achieve significantly improved prognosis for patients with MBCs. At the completion of this project, it is expected
that the anti-metastasis and life-prolonging efficacy of HJC0152 will b...

## Key facts

- **NIH application ID:** 10017168
- **Project number:** 5R01CA231150-03
- **Recipient organization:** LSU HEALTH SCIENCES CENTER
- **Principal Investigator:** Qiang Shen
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $1
- **Award type:** 5
- **Project period:** 2018-07-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10017168

## Citation

> US National Institutes of Health, RePORTER application 10017168, Targeting Glucose Metabolism with HJC0152 for Treating Metastatic Breast Cancer (5R01CA231150-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10017168. Licensed CC0.

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